Purpose:
Sulforaphane, a natural isothiocynate presented in cruciferous vegetables, is known as activator of transcription factor Nrf2 which activates genes encoding for antioxidative enzymes. In this study, we evaluate the effect of sulforaphane to protect the retina cells in vitro and retina function in vivo.

Methods:
ARPE-19 cells was pretreated with sulforaphane following by adding tert-butyl hydroperoxide. Cell viability was evaluated by MTT assay. ROS production and mitochondrial dysfunction were measured by ROS assay and JC-1 Mitochondrial Membrane Potential Assay, respectively. Antioxidative enzymes (HO-1, GR, GPx1, NQO1) and proinflammatory mediators (ICAM-1, MCP-1) were quantified by PCR and western analysis. For in vivo study, Sprague-Dawley rats were randomized to receive saline, low-dose or high-dose sulforaphane treatment before ischemia reperfusion (IR) injury. ERG was used to measure retinal function. ROS production with retina was evaluated. EMSA were used to check the activation of Nrf2 and NF-kB in retinal cells.

Conclusions:
Treatment of ARPE 19 cell with sulforaphane effectively protected cells against oxidative stress by activated the Nrf2-dependent proteins to increase the anti-oxidative effect. Sulforaphane also preserved the retina function after IR injury in vivo. These results supported that sulforaphane had the cytoprotective effect against oxidative stress and may be useful in combating human acute retinal IR injury.